Notwithstanding recent advances in direct
antiviral specialists (DAAs) for
hepatitis C infection (HCV), it is yet a pervasive overall issue in patients with
rheumatoid arthritis (RA). Exosomal
microRNAs (
miRNAs) is associated with HCV
infection. However, it remains unknown how
miRNAs respond following biologic
disease-modifying antirheumatic drug (bDMARD) and targeted synthetic
DMARD (tsDMARD) treatment in HCV patients with RA. We prospectively recruited RA patients taking anti-
tumor necrosis factor-α (TNF-α) inhibitors
rituximab (RTX) and
tofacitinib. The serum
hepatitis C viral load was measured using real-time quantitative
reverse transcriptase PCR before and 6 months after bDMARD and tsDMARD
therapy. HCV RNA replication activity was measured using an HCV-tricistronic replicon reporter system, and quantitative analysis of hsa-mir-122-5p and hsa-mir-155-5p in patients was performed using quantitative PCR. HCV RNA replication in hepatocytes was not affected by
tofacitinib or TNF-α inhibitor treatment. Hsa-mir-155-5p and hsa-mir-122-5p were significantly expanded in RA patients with HCV as compared with those without HCV. We observed a dramatic increase in hsa-mir-122-5p and a decrease in hsa-mir-155-5p expression levels in patients taking RTX in comparison with other treatments. Finally, a reduction in hsa-mir-122-5p and an increase in hsa-mir-155-5p were observed in a time-dependent manner after
tofacitinib and DAA
therapy in RA-HCV patients. These results showed that hsa-mir-155-5p and hsa-mir-122-5p were significantly increased in RA-HCV patients as compared with those without HCV after taking
tofacitinib. Hsa-mir-155-5p and hsa-mir-122-5p may be potential
biomarkers for treatment efficacy in RA patients with HCV.